Elucidating How Chondrocytes Maintain Cartilage Stability
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 20 February 2026 | Viewed by 480
Special Issue Editor
2. Roy J. Carver Department of Biomedical Engineering, College of Engineering, University of Iowa, Iowa City, IA 52242, USA
3. Division of Pharmaceutical Sciences and Experimental Therapeutics, College of Pharmacy, University of Iowa, Iowa City, IA 52242, USA
Interests: orthopaedics; chondrocytes; osteoarthritis; arthrofibrosis; tissue engineering
Special Issue Information
Dear Colleagues,
The overall goal of this Special Issue is to address knowledge gaps that stand in the way of developing novel chondrocyte-based interventions to prevent, forestall, or reverse articular cartilage degeneration.
The unique physiologic adaptations that allow chondrocytes to maintain cartilage homeostasis are incompletely understood, as are the factors that disrupt homeostasis and lead to degeneration. Given the complexity of these processes, the way forward will likely involve detailed molecular analyses of data from cell and tissue culture models, as well as from animal models.
Significant knowledge gaps include the following:
- Mechano-transduction: While it is common knowledge that chondrocytes modulate ECM turnover in response to mechanical stresses, the signal transduction pathways that mediate these effects have not been fully elucidated.
- Inter-cellular communication: Chondrocyte activities are profoundly influenced by factors secreted by other joint cells, including synoviocytes and bone cells. Research in other domains indicates that extracellular vesicles (EVs) play a major role in cell-to-cell communication; however, relatively little is known regarding the role of EVs in maintaining or disrupting cartilage homeostasis.
- Cartilage repair/regeneration: Although stem and resident progenitor cells can be coaxed to produce a cartilage-like tissue, it is unclear to what extent this results in a fully functional, resilient ECM.
- Chondrocyte aging: Age-related increases in chondrocyte apoptosis diminish cellularity, resulting in declines in the ability of chondrocytes to maintain cartilage homeostasis. However, there also appear to be metabolic changes associated with aging that disrupt homeostasis.
- Therapeutic delivery: Efficient targeting of chondrocytes in vivo with minimal off-target effects will require advanced vehicles designed specifically for rate-controlled intra-articular delivery.
Dr. James A. Martin
Guest Editor
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Keywords
- chondrocytes
- articular cartilage
- chondrogenesis
- osteoarthritis
- mechano-transduction
- aging
- extracellular matrix
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